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Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat.

Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Research Abstract Details 

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  • Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Abstract Text:

    stacy m townsendStacy M Townsend,edward hurrellEdward Hurrell,ignacio gonzalez-gomezIgnacio Gonzalez-Gomez,james loweJames Lowe,jonathan g fryeJonathan G Frye,stephen forsytheStephen Forsythe,julie l badgerJulie L Badger,

    Enterobacter sakazakii is an opportunistic pathogen associated with contaminated powdered infant formula and a rare cause of Gram-negative sepsis that can develop into meningitis and brain abscess formation in neonates. Bacterial pathogenesis remains to be fully elucidated. In this study, the host inflammatory response was evaluated following intracranial inoculation of Ent. sakazakii into infant rats. Infiltrating macrophages and neutrophils composed multiple inflammatory foci and contained phagocytosed bacteria. Several genotypically distinct Ent. sakazakii strains (16S cluster groups 1-4) were shown to invade rat capillary endothelial brain cells (rBCEC4) in vitro. Further, the persistence of Ent. sakazakii in macrophages varied between strains. The presence of putative sod genes and SOD activity may influence the survival of acidic conditions and macrophage oxidase and contribute to Ent. sakazakii intracellular persistence. The influence of macrophage uptake of Ent. sakazakii on immunoregulatory cytokine expression was assessed by ELISA. This demonstrated that the IL-10/IL-12 ratio is high after 24 h. This is suggestive of a type 2 immune response which is inefficient in fighting intracellular infections. These findings may help explain how the diversity in virulence traits among Ent. sakazakii isolates and an unsuccessful immune response contribute to the opportunistic nature of this infection.

    Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Publishing Authors By Initials

    sm townsendSM Townsend,e hurrellE Hurrell,i gonzalez-gomezI Gonzalez-Gomez,j loweJ Lowe,jg fryeJG Frye,s forsytheS Forsythe,jl badgerJL Badger,

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    Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Microbiology (Reading, England)

    VOLUME: 153

    Page Numbers: 3538-47

    Journal Abbreviation: Microbiology (Reading, Engl.)

    ISSN: 1350-0872

    DAY: 27

    MONTH: Oct

    YEAR: 2007

    Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Information

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    LANGUAGE: eng

    NlmUniqueID: 9430468

    Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat. Keywords Mesh Terms:

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    Grant and Affiliation Information for Enterobacter sakazakii invades brain capillary endothelial cells, persists in human macrophages influencing cytokine secretion and induces severe brain pathology in the neonatal rat.

    AFFILIATION: School of Biomedical and Natural Sciences, Nottingham Trent University, Clifton Lane, Nottingham NG11 8NS, UK. stacy.townsend@hotmail.com

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: Microbiology

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